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3 Session B: Health Effects of Lead ."
Lead in the Americas: A Call for Action . Washington, DC: The National Academies Press,
1996 .

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LEAD IN THE AMERICAS: A call for action
SESSION B
Health Effects of Lead

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LEAD IN THE AMERICAS: A call for action
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LEAD IN THE AMERICAS: A call for action
EFFECTS OF LEAD ON CHILDREN'S HEALTH
EDUARDO PALAZUELOS-RENDÓN*
SOURCES AND PATHWAYS OF LEAD POISONING IN CHILDREN
The use of lead dates back some 7,000 years in such activities as mining, pottery, glasswork, and the production of cosmetics. Its use has broadened in modern times and now extends to the production of paints and the chemical, petroleum refinery, and automotive industries.
Unfortunately, lead is also an element that serves no vital function in the human organism and is one that is toxic, even in the smallest amounts. Humans have utilized lead in such abundance and for so long that levels of lead have been found in minuscule amounts in almost all populations surveyed. This, sadly, has made it possible to talk about a “normal” lead level in humans.
Sources of lead exposure in humans can be classified into two groups, according to the population affected. One source derives from occupational and industrial sources and the other from “domestic” sources, where the target population includes nonworking adults and children, and the exposure levels are influenced by the environment, customs, and habits of that population. Control and prevention strategies to address domestic sources of lead exposure are more complex than those for confined occupational sources, because of the former's varied, heterogeneous nature (Landrigan, 1988).
The major domestic sources contributing to increased blood lead levels in children in most countries of the Americas are vehicular traffic and air pollution caused by use of leaded gasoline (Romieu et al., 1992). Other important sources include use of earthenware that contains lead, leaded paint in residential housing, and consumption of water from pipelines and food stored in tin cans that contain leaded solder (Hernberg, 1975;
*
Minister of the Environment, Mexico City, Mexico

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Jiménez et al., 1993; Lara-Flores et al., 1989; Schwartz and Levin, 1991;Tackett, 1987). Indirect exposures to lead hazards are also probably common to children in many countries of the Americas. In Mexico City, for example, a case of indirect lead poisoning was reported in a clinical session at the Hospital Infantil de México Federico Gómez in April 1995. The case, a 3-year-old child of low socioeconomic status from a rural community, was admitted with neuroencephalopathy and convulsions of 24 hours duration and with a history of eight days of vomiting not related to food or liquid consumption. The patient died five days after admission without a diagnosis. The only relevant information in the patient's history that indicated potential lead exposure was that the child was the daughter of potters. The diagnosis of acute lead poisoning was made by autopsy. This is a rare and extreme event associated with lead poisoning and illustrates the lack of awareness that lead is an important public health problem.
The major pathway of exposure in children is through the digestive system. Young children characteristically explore their environment with their hands and mouths and, as a result, many children consume items not normally eaten, such as leaded paint chips, a behavior called pica (Barltrop and Khoo, 1975; Johnson and Tenuta, 1979). In addition, children absorb lead at a higher rate than adults: children absorb about 50 percent of the lead in their diets; adults have an absorption rate of approximately 5 to 10 percent (Mahaffey, 1981). The total amount of lead consumed can also influence absorption rates in children. Mahaffey (1981) has shown, for example, that when the amount of lead in the diet is greater than 5 mg/kg of body weight, children absorb and retain relatively more lead.
The sources of lead ingested by children differ according to the time, region, and group of children studied. For example, principal sources of lead poisoning in children were reported to include ingested household dust contaminated with lead brought home by parents who are industrial workers in Memphis, Tennessee (Baker et al., 1977); contaminated soil in an area near a lead smelter in Santo Amaro, Brazil (Silvany-Neto et al., 1989); household leaded paints and lead-containing tap water in Boston, Massachusetts (Shannon and Graef, 1992); and contaminated dust from factories producing lead-containing ceramics in the Umbria region of central Italy (Abbritti et al., 1992).
Research has shown that the consumption of certain nutrients in the diet—including minerals such as calcium, phosphorus, iron, and zinc and vitamins such as vitamins C, E, and thiamin—can reduce absorption of dietary lead in children (Mahaffey, 1990). Nutrition education directed

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toward increasing the levels of these nutrients in the diet may, therefore, be a useful intervention in situations where dietary lead levels are characteristically low.
EVOLUTION IN CLINICAL UNDERSTANDING OF THE DANGERS OF LEAD POISONING IN CHILDREN
The evolution in clinical understanding of the dangers of lead toxicity in children had two defining moments. The first occurred at the end of the nineteenth century with the recognition that lead is a poison. This understanding derived from a clinical case series of children with high blood lead levels in Australia who exhibited concomitant symptoms of paralysis and opthalmoplegia (Needleman, 1988, 1992b). Prevention and control strategies, in response, focused on rapid identification of exposed populations (primarily industrial), description of the sources of poisoning, and attempts to reduce the acute effects of intoxication. Following this report, the orientation of public health interventions was directed toward study and control of severe lead poisoning and its associated health effects, including plumbic colic, encephalopathy, anemia, and renal illness. The more subtle adverse effects now known to be associated with lower exposure levels remained unrecognized until more recently (Goyer, 1990).
The second phase was initiated in the 1960s with the development of biologic markers for low exposure levels and clinical identification of associated adverse health effects. These advancements changed the clinical and public health paradigm of lead poisoning to one of widespread acceptance that no level of lead exposure could be considered safe. Figure 3-2 reflects current understanding of the adverse health affects associated with increasing blood lead levels.
The growing recognition of lead's dangerous effects has led to a gradual reduction in acceptable blood lead levels. In 1960, for example, the acceptable limit was 60 µg/dl; limits subsequently dropped, to 40 µg/dl in 1971 and 30 µg/dl in 1975. By 1985, the limit in Mexico was lowered to 25 µg/dl; by 1990, the highest acceptable level of lead in blood was 15 µg/dl. Accumulating epidemiologic data now convincingly demonstrate neurotoxicity in children exposed to lead at levels below 15 µg/dl and, as a result, the U.S. Centers for Disease Control and Prevention (CDC) have now lowered their acceptable blood lead limit to 10 µg/dl (CDC, 1991).
The decline in acceptable levels was prompted, in large part, by the increasing sophistication of screening methods. Biologic markers that

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Figure 3-2. Effects of inorganic lead on children and adults—lowest observable adverse health effects. Source: ATSDR, 1992.

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have been used in surveys of children include lead in blood, teeth, hair, and bone. Blood lead is the most commonly used indicator, and it has been the basis for most of the studies that have established cause-and-effect relationships between lead exposure and disease. The level of lead in blood reflects, biokinetically, both the degree of relatively recent exposure to lead and the toxicologically active fraction of the total body load of lead in various tissues, at least in stable conditions. Blood lead levels are more labile in childhood and tend to become more stable with age.
Values of lead in hair, teeth, and bone provide a measure of accumulated exposure over time. Of the three, lead in hair represents perhaps the most useful biologic indicator because its samples are noninvasive, can be stored indefinitely, and can provide temporal clues to exposure through sampling across the length of the hairshaft.
SYMPTOMS AND SIGNS OF SEVERE LEAD POISONING IN CHILDREN
In children without encephalopathy, lead poisoning is characterized by one or more of the following symptoms: reduction in play activity, lethargy, anorexia, sporadic vomiting, intermittent abdominal pain, and constipation. In cases of acute lead poisoning, encephalopathy may present at diagnosis with the following symptoms: coma, convulsions, behavioral disturbances, apathy, lack of coordination, vomiting, alteration in consciousness, and loss of recently learned abilities (Piomelli et al., 1984). Studies of lead-induced encephalopathy indicate that blood lead levels must be very high (90 to 400 µg/dl) to produce clinical signs of encephalopathy such as hyperactivity, ataxia, convulsions, stupor, and coma. Blood lead levels of 60 to 300 µg/dl may produce encephalopathic-like signs and symptoms that are often confused with true encephalopathy (Grant and Davis, 1989). In recent years, researchers have reported extensive results on the developmental and neuropsychological effects of lead in children (Needleman and Gasonis, 1990; Pocock et al., 1987).
Lead is a neurotoxic that adversely affects neurodevelopment of children. Groups of children at high risk of lead exposure have been shown to have lower intelligence scores, depending on the type of evaluative test used. Although these findings continue to be challenged by an increasing minority of clinicians and researchers, there is a rapidly accumulating base of evidence that suggests that blood lead levels are inversely related to cognitive function and ability (Bentou-Maranditou et al., 1988; Hansen et al., 1989; Landrigan, 1989; Needleman and Gatsonis, 1990; NRC, 1993;

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Rabinowitz et al., 1991). Studies have also indicated inverse associations between body lead levels and neuroconductivity (Fergusson et al., 1993; Grandjean et al., 1991; Stiles and Bellinger, 1993), motor-visual integration (Baghurst et al., 1995; Bellinger, 1995), and behavioral problems reported by teachers and parents (Silva et al., 1988).
In 1993, Muñoz and colleagues (1993) reported findings of a study evaluating neurocognitive development capacity in children in Mexico City with chronic lead exposures. Their results showed that the average blood lead levels of their study sample exceeded 19 µg/dl and that the major sources of exposure were vehicular traffic near the child' s residence, use of glazed pots for preparing or storing food or juices, and frequency of chewing pencils. Blood lead levels were a strong predictor of lower performance on full-scale IQ as measured by a version of the Wescheler Intelligence Scale for Children (WISC), as well as lower scores on other measures of school performance.
Studies of prenatal blood lead levels as predictors of future neurologic and behavioral development of the fetus and child are of increasing interest. One of the elements that has permitted this line of research is the ability to evaluate fetal exposure to lead through measurements of the umbilical cord blood and bone lead of the mother. For example, Bellinger and colleagues (1984, 1986) reported neurobehavioral deficits on the Bayley Scale of Infant Development associated with higher prenatal exposures (cord blood lead levels of 10–25 µg/dl). The observed deficits persisted until two years of age, although postnatal exposures of all children in the study cohort were comparable. Further study of these children suggested that the neurobehavioral differences associated with the high cord blood levels were strongly attenuated by the time the children reached preschool age (Bellinger, 1991). Values obtained from such indicators of early exposure from cord blood levels will provide a basis for many ongoing cohort studies evaluating early lead exposure and neurologic outcome.
Autopsy studies indicate that bone is the primary site of storage for about 95 percent of lead in the human body. It is known that pregnancy and lactation create a significant demand for calcium and that this calcium is, in part, provided from bone, a process that causes the concomitant release of accumulated lead. Studies that incorporate consideration of blood lead levels as a source of exposure will thus increase the ability to assess the deleterious effects of maternal lead burden in the newborn.

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CONCLUSIONS
Children continue to be exposed to lead across the Americas, although the sources and pathways of exposure differ across and within countries. In Mexico, as in many other countries of the region, a major hurdle remains the need to convince the health authorities of the extent and seriousness of childhood lead poisoning. To move toward this end, there is a need for more extensive identification and monitoring of lead levels in high-risk children and for the strengthening of medical education to alert pediatricians and other clinical practitioners to the signs, symptoms, and effects of lead poisoning. Blood lead levels should be measured at least once in high-risk children in the first year of life, and clinic personnel should be prepared to provide basic counseling to parents on how to reduce infant and child exposure to lead. Special attention should be directed toward reducing domestic sources of exposure—for example, through education about the dangers of using leaded ceramics in food preparation and storage.

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EFFECTS OF LEAD ON ADULT HEALTH
JULIETA RODRÍGUEZ DE VILLAMIL*
Lead poisoning continues to be one of the most prevalent occupational, paraoccupational, and environmental illnesses affecting adults. No metal has been more extensively studied from the epidemiologic, clinical, and toxicologic perspectives (see Saryan and Zenz, 1994). Unfortunately, clinical diagnosis of lead poisoning in the adult is often complicated by the variability and indistinctiveness of the presenting symptoms and signs. Correct diagnosis of a lead-poisoned individual, therefore, requires adequate clinical training, the execution of a complete occupational and environmental history, laboratory facilities for lead determination, and awareness of the problem by health care professionals.
An understanding of the problem of lead poisoning in adults requires that specific factors that predispose or aggravate lead's effects be taken into account. Examples of such factors are:
the concentration and type of lead (inorganic lead vs. alkyl lead) in the source of exposure;
the duration of exposure;
the route of entrance into the adult;
the underlying nutritional status and health of the individual;
the age of the individual exposed;
the health-related habits/behaviors of the person exposed (for example, cigarette smoking in a contaminated environment);
the race and sex of the person exposed.
The combination of these factors will influence the susceptibility of the exposed person and the nature and extent of his or her disease. It will also influence the choice of strategies to best prevent or control a given environmental or occupational exposure.
*
Under-Minister of Occupational Health, Bogota, Colombia

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RECOGNITION OF THE PROBLEMA
By the time that Hippocrates first described symptoms of lead poisoning in metal workers, physicians were aware of the lethal effects of inhaling lead fumes and methods of protection for workers. At that point, however, the Romans used lead widely for cosmetics, wine reservoirs, and construction of aqueducts and cisterns (Kazantzis, 1989). In the early twentieth century, Alice Hamilton described symptoms of lead poisoning in painters and other artisans whose paints were lead-based (Hamilton and Hardy, 1949). This was followed by a growing number of monographs, worldwide, that described similar symptoms and signs in other occupational groups exposed to lead.
ROUTES OF EXPOSURE
The major routes of absorption of lead are the gastrointestinal tract and the respiratory system. Skin absorption of lead is generally insignificant; when lead is in the form of lead alkyl compounds (such as tetraethyl lead), however, it can be absorbed readily by the skin.
Once lead particulates are deposited in the lower respiratory tract, they are rapidly and completely absorbed. The rate of deposition varies according to the particulate size and the ventilation rate. As a rule, in the adult, between 30 and 50 percent of lead is absorbed.
Lead ingestion also results from consuming food and beverages contaminated with lead and from swallowing lead particulates cleared by the upper respiratory tract. The absorption of lead by the gastrointestinal tract appears to be low in adults, but not in children, as is indicated in the previous report by Dr. Eduardo Palazuelos-Rendón. Gastrointestinal absorption is increased by dietary deficiencies of calcium, iron, potassium, and zinc. For the forms of lead in the normal diet, absorption is also increased by fasting. Absorption rates can vary from a high of 45 percent in fasting conditions to a low of 6 percent in the presence of food.
Lead, whether absorbed through the gastrointestinal tract or the respiratory system, is distributed in essentially the same fashion into blood, bone, and soft tissues. Figure 3-3 depicts the metabolism of lead in the human system.
Blood lead is the biological marker most commonly used to assess lead exposure. Approximately 3 percent of the total body burden of lead circulates in the blood. Within the circulatory system, the majority of

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Figure 3-3. Simplified model of the metabolism of lead in man. Source: Hernberg, 1988.

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lead (around 50 percent) is associated with hemoglobin, and only a small and variable fraction (depending on a nonlinear relation to the whole blood lead level) is free in plasma. This biologically active fraction of lead—which is able to cross the placental and hematoencephalic barriers—is considered to be the fraction that contributes to immediate toxicity. Lead in blood has the shortest half-life, estimated to be between 28 and 36 days, followed by lead in soft tissue (46 days), and lead in bone (20 years or more).
Autopsy studies indicate that lead accumulates in bone throughout life. Bones serve as a long-term repository of approximately 75 percent and 95 percent of lead in children and adults, respectively (Barry and Mossman, 1970). Studies have demonstrated that bone lead levels remain elevated despite declines in blood lead, suggesting that bone lead may be a better biological marker of chronic toxicity (Steenhout, 1982). Indirect evidence has shown that lead is continually released from bone stores, but particularly so during times of increased bone turnover such as pregnancy, breastfeeding, and menopause (Silbergeld, 1991). Therefore, as indicated in the previous paper by Dr. Eduardo Palazuelos-Rendón, there is concern that—in addition to affecting the adult woman—a significant amount of bone lead may be transferred to the fetus or to the breastfed infant.
EXCRETION
Data suggest that in adults constantly exposed to lead, between 50 and 60 percent of the absorbed fraction of lead is excreted within 15 days. Excretion occurs predominantly through urine and, in minor quantities, through bile and exfoliation of epithelial tissue.
HEALTH EFFECTS
Hematopoetic Effects
Lead has long been known to affect heme biosynthesis by inhibiting the δ-aminolevulinic acid dehydratase (ALA-D). Microcytic anemia is one of the early manifestations of lead poisoning —abnormalities in the peripheral blood smear include microcytes with stippling Cabot's rings. In occupationally exposed adults, however, the blood lead threshold level for a decrease in hemoglobin is estimated to be 50 µg/dl.

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Neurological Effects on the Central and Peripheral Nervous Systems
Acute encephalopathy is commonly seen when ambient air concentrations of lead are higher than 10 mg/m3 and when blood lead levels exceed 100 µg/dl. Chronic encephalopathies associated with lower levels of lead exposure are characterized by changes in mental activity and cognitive function, hyperirritability, disassociation, depression, and headaches, while higher blood lead levels have been associated with vertigo, ataxia, convulsions, explosive vomiting, and stupor. Severe sequelae include blindness, mental retardation, mental dysfunction, epilepsy, neurobehavioral disruptions, coma, and death.
Peripheral neuropathy—characterized by cutaneous hypersensitivity, tremors, weakness, hypotonia, and muscular atrophy—has been associated with lead exposure, although a clear dose-response relationship has not been demonstrated. Compromised radial nerve function and “horse foot” (compromised fibula nerve function) have also been frequently described in lead poisoning victims. Subclinical states have also been described in asymptomatic adults with lead levels between 80-120 µg/dl and have been characterized by diminished conductor velocity, muscular fibrillation, and loss of motor neurons.
Renal Effects
Acute renal effects include reversible loss of renal function—damage to the proximal tubules, which produces a Fanconi Syndrome manifested by aminoaciduria, glucosuria, and phosphaturia. Continuous, prolonged high lead exposure results in chronic and nonreversible effects associated with progressive interstitial fibrosis, which may lead to renal damage characterized by interstitial fibrosis, sclerosis of vessels, glomerular atrophy, reduced glomerular filtration, and azotemia.
Cardiovascular Effects
There is considerable debate as to whether there is a causal association between lead exposure and hypertension (Hertz-Picciotto and Croft, 1993). Large-scale mortality studies of occupationally exposed individuals have strongly supported the association between lead and hypertension. Schwartz estimated that in the United States, 24,000 cases of myocardial infarction yearly could be eliminated if blood lead levels were reduced by 50 percent

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(Schwartz, 1991). In contrast, most studies in the general population have reported small effects on blood pressure, or no association at all. Taken together, the evidence does not provide conclusive evidence that lead exposure is positively associated with hypertension. More studies are needed, especially longitudinal studies that use new biomarkers for cumulative exposure, and serial measurements to evaluate recent exposure.
Gastrointestinal Effects
Colic is a consistent early symptom in occupationally exposed cases or in cases of acute intoxication. Initial nonspecific symptoms appear at blood lead levels of approximately 80 µg/dl, and include dyspepsia, anorexia, postprandial epigastritis, constipation, cramps, and nausea. Gastrointestinal symptoms are aggravated when blood lead levels reach 100 µg/dl or higher and can include severe abdominal colic and constipation. Severe symptoms occur at blood lead levels of 150 µg/dl or higher and can include “lead colic” (severe abdominal spasms that resemble acute abdominal pain requiring surgery) and liver damage.
Skeletal Effects
Formation of lead triphosphate binds lead to bone. This “hidden” accumulation is released during the demineralization of bone that occurs in the normal metabolic processes of aging and pregnancy. The release of “hidden” lead during pregnancy and that unbound lead is present in mother's milk is of particular concern given the increased risks this poses to the fetus and infant.
Reproductive Effects
A large number of reports indicate that high levels of lead exposure are associated with impaired fertility in both women and men (Rom, 1976). Several studies have reported an increase in miscarriage, stillbirth, low birthweight, and other abnormalities associated with high exposures at industrial levels. Low-level exposure in utero has been associated with higher prevalence of low birthweight, reduced head circumference, and reduced length at birth (Coste et al., 1991; Lancrajan, 1975).

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Carcinogenic and Genotoxic Effects
Other effects related to lead exposure include genotoxic and carcinogenic effects. Data suggest that exposure to organic lead can result in changes in lymphocyte chromosomes. In relation to carcinogenic effects, lead by-products, including phosphate and lead acetate, are known to cause renal cancer in laboratory animals, although this has not been proven in humans.EXPOSURE INDICATORS
Plumbism (although there are no associated pathogenic signs and symptoms) can be used as an indicator of recent exposure, although symptoms and signs are often vague and nonspecific. Levels of lead in urine exceeding 150 µg/dl can be diagnostic of lead poisoning.
Blood levels of erythrocyte protoporphyrin (ZPP) correlate well with lead exposure and provide a useful indicator for general population screening, but can be inaccurate in cases of iron deficiency. Levels of ZPP and their blood lead equivalents are presented in Table 3-2.
Clinical Tests
Lead can be measured in blood, serum, urine, tissues, teeth, bone, and hair. All of these indicators provide reliable information about exposures and health risks associated with exposure. Tests that are useful in the diagnosis of lead poisoning are:
TABLE 3-2
Levels of ZPP and Blood Lead Level Equivalents
ZPP (mg/100 ml)
Interpretation
Blood Lead Level Equivalents
< 80
Normal for adults
—
80–250
Typical labor exposure
20–40 mg/100ml
251–500
High range of exposure
40–55
> 500
Extreme exposure
> 55
Source: Adapted from Saryan and Zenz, 1994.

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ALA-D: Normal levels in urine are 6 µg/dl. This test has limited utility because of its high cost.
Urinary coproporphyrin >500 µg/dl.
Electrophysiological tests of conduction velocity, evoked potential.
Tests of neuroconductivity. These are of particular use in evaluating children.
Radiological exams of long bones (lead line) and abdomen (for radiopaque paint), and, recently, X-Ray Fluorescence, have been found useful in determining levels of sequestered lead in bone.
Clinical Examination
Clinical examination of cases of suspected lead poisoning should include a detailed history of possible environmental and occupational exposure to lead; a complete physical examination, especially of blood pressure; laboratory tests of blood lead, hematic cytology, hemoglobin, BUN, and creatine; and urinalysis.
Treatment
The first step in treatment must be to identify the source of patient exposure, to identify other family members or coworkers with a similar exposure, and to intervene immediately to stop exposure. Vomiting should be induced in cases of recent lead ingestion; the use of coal, other carbon, or cathartics is not of proven efficacy. Symptomatic treatment should be applied in cases of encephalopathy. The use of chelation therapy with such agents as calcium disodium edetate ( EDTA), British antilewisite (BAL), d-penicillamine (DMPS), and/or succimer (DMSA) Can be useful in cases of severe lead poisoning. The cost of these therapies is high, however, and use of these agents has associated undesirable side effects (Frumkin, in press).
CONCLUSIONS
The multisystemic effects, prolonged half-life in the human organism, and chronicity of lead poisoning underscore its seriousness as a public health problem and illustrate the need to focus public health attention on prevention as a first priority.
Lead is ubiquitous in the environment. As a result, detection, prevention, and control strategies need to be directed to domestic as well as

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occupational sources. The responsibility of controlling lead exposures and guaranteeing healthy working and living conditions must be shared by everyone, including government, workers, unions, scientists, health providers, and the general public.

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